The mechanisms responsible for myocardial hibernation have yet to be elucidated, despite numerous investigation. Two road types of animal models have been utilized: 1.) Acute or short-term hibernation, which involves a coronary stenosis for 90 minute duration 2.) chronic hibernation with coronary stenosis > 2-3 weeks. Recent studies from Dr. S Vatner's laboratory found that 1.) Chronic coronary stenosis induced by ameroid coronary constriction in swine results in several features of hibernating myocardium in humans, but does not results in reduced blood flow at rest despite significant reduction in function, 2.) short-term coronary stenosis (1.5 hr) results in a protective effect mediated by up- regulation of nitric oxide (NO) function, and 3.) myocardial blood flow in woodchucks during true hibernation is also maintained despite reduction of apparent metabolic demand, i.e., temperature and heart rate, and visceral flow reductions ranging from 80-90%. Specifically, this application will address the following hypotheses related to the maintenance of myocardial blood flow and myocardial performance in models of "short-term", "chronic" and "true" hibernating myocardium: 1.) Coronary stenosis induces an up-regulation of NO production that is protective during a sustained coronary stenosis in a model of acute hibernating myocardium, and that this protective mechanism is mediated by cardiac nerves. 2.) Hibernating myocardium can result from chronic stunning. 3.) Coronary blood flow is maintained in a model of chronic hibernating myocardium, i.e., during long-term coronary stenosis with ameroid coronary constriction in swine, potentially due to NO up- regulation of NO. 4.) Coronary blood flow is maintained in true hibernating myocardium in woodchucks, potentially due to up-regulation of NO. The work in this project is closely related to work in the other projects, which utilize similar models, and to all of the Cores.